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Autoimmunity against INS-IGF2 Protein Expressed in Human Pancreatic Islets
Lund University.ORCID iD: 0000-0002-9953-2829
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2013 (English)In: Journal of Biological Chemistry, ISSN 0021-9258, E-ISSN 1083-351X, Vol. 288, no 40, p. 29013-29023Article in journal (Refereed) Published
Abstract [en]

Insulin is a major autoantigen in islet autoimmunity and progression to type 1 diabetes. It has been suggested that the insulin B-chain may be critical to insulin autoimmunity in type 1 diabetes. INS-IGF2 consists of the preproinsulin signal peptide, the insulin B-chain, and eight amino acids of the C-peptide in addition to 138 amino acids from the IGF2 gene. We aimed to determine the expression of INS-IGF2 in human pancreatic islets and autoantibodies in newly diagnosed children with type 1 diabetes and controls. INS-IGF2, expressed primarily in beta cells, showed higher levels of expression in islets from normal compared with donors with either type 2 diabetes (p = 0.006) or high HbA1c levels (p < 0.001). INS-IGF2 autoantibody levels were increased in newly diagnosed patients with type 1 diabetes (n = 304) compared with healthy controls (n = 355; p < 0.001). Displacement with cold insulin and INS-IGF2 revealed that more patients than controls had doubly reactive insulin-INS-IGF2 autoantibodies. These data suggest that INS-IGF2, which contains the preproinsulin signal peptide, the B-chain, and eight amino acids of the C-peptide may be an autoantigen in type 1 diabetes. INS-IGF2 and insulin may share autoantibody-binding sites, thus complicating the notion that insulin is the primary autoantigen in type 1 diabetes.

Place, publisher, year, edition, pages
2013. Vol. 288, no 40, p. 29013-29023
National Category
Cell and Molecular Biology Immunology in the medical area
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URN: urn:nbn:se:hkr:diva-12676DOI: 10.1074/jbc.M113.478222ISI: 000330298800055PubMedID: 23935095OAI: oai:DiVA.org:hkr-12676DiVA, id: diva2:739646
Available from: 2014-08-21 Created: 2014-08-21 Last updated: 2018-01-11Bibliographically approved

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Vaziri-Sani, Fariba

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CiteExportLink to record
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